# Contemporary Assessment and Management of Effusive-Constrictive Pericarditis

**Authors:** Lamis El Harake, Ashraf Samhan, Paul C. Cremer, Mohamed Al Kazaz

PMC · DOI: 10.1007/s11886-025-02326-4 · 2026-01-21

## TL;DR

This review discusses the diagnosis and treatment of effusive-constrictive pericarditis, a heart condition involving fluid buildup and restricted heart function.

## Contribution

The paper provides updated insights into the management of ECP using multimodal imaging and targeted therapies based on etiology.

## Key findings

- Echocardiography is now the primary diagnostic tool for ECP, allowing early detection of constrictive physiology.
- Inflammatory ECP often responds to anti-inflammatory drugs, while tuberculous cases require antimicrobial therapy with corticosteroids.
- Pericardiectomy is reserved for irreversible cases unresponsive to medical treatment.

## Abstract

Effusive-constrictive pericarditis (ECP) is a complex clinical condition that combines features of pericardial effusion/tamponade and constrictive pericarditis. The classic hemodynamic definition is persistent elevation of right atrial pressure despite drainage of a pericardial effusion. This review summarizes recent data on its epidemiology, pathophysiology, diagnosis, and management.

Prevalence varies from 2.4% to 14.8% depending on diagnostic criteria and etiology, reaching up to 50% in tuberculous pericarditis in endemic regions. Common causes include idiopathic, infectious (particularly tuberculous and bacterial), malignant, and post-surgical etiologies. While invasive hemodynamic assessment remains the reference standard, echocardiography is now the primary diagnostic tool, enabling recognition of constrictive physiology before and after pericardiocentesis. Cardiac magnetic resonance adds complementary information on pericardial thickness, inflammation, and potential for reversibility, aiding therapeutic decisions. Inflammatory ECP frequently resolves with medical therapy (NSAIDs, colchicine, corticosteroids, or IL-1 inhibitors) while tuberculous cases require antimicrobial therapy with corticosteroids in selected patients.

ECP is a heterogeneous condition with variable clinical trajectories. Early identification through multimodality imaging is essential to guide therapy, target reversible inflammation, and prevent chronic constriction. Most inflammatory cases respond to anti-inflammatory treatment, whereas pericardiectomy is reserved for persistent, irreversible constrictive physiology despite optimal medical therapy.

The online version contains supplementary material available at 10.1007/s11886-025-02326-4.

## Linked entities

- **Chemicals:** colchicine (PubChem CID 2833)
- **Diseases:** tuberculous pericarditis (MONDO:0005903)

## Full-text entities

- **Genes:** IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, RNASE3 (ribonuclease A family member 3) [NCBI Gene 6037] {aka ECP, RAF1, RNS3}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}
- **Diseases:** heart failure (MESH:D006333), death (MESH:D003643), inferior vena cava dilation (MESH:C563013), pericardial compressive syndromes (MESH:D009408), edema (MESH:D004487), calcifications (MESH:D002114), Chest pain (MESH:D002637), myocardial involvement (MESH:C564676), HIV-associated malignancies (MESH:D016263), chronic effusions (MESH:C564895), hepatomegaly (MESH:D006529), CTP (MESH:D002305), Effusive (MESH:D000080324), Chronic inflammation (MESH:D007249), fever (MESH:D005334), tachycardia (MESH:D013610), primary right ventricular failure (MESH:D051437), CP (MESH:D010494), Pericarditis (MESH:D010493), dyspnea (MESH:D004417), dry (MESH:D015352), Tuberculous pericarditis (MESH:D010495), systemic (MESH:D015619), Pericardial effusion (MESH:D010490), autoimmune (MESH:D001327), Kaposi sarcoma (MESH:D012514), EC (MESH:D005955), ascites (MESH:D001201), Malignant effusions (MESH:D016066), hypotension (MESH:D007022), diastolic chamber collapse (MESH:D006337), pericardial thickening (MESH:D013585), tuberculosis (MESH:D014376), tricuspid regurgitation (MESH:D014262), vena cava (MESH:D013479), TB (MESH:D014390), IVC dilation (MESH:C567679), HIV co-infection (MESH:D015658), fatigue (MESH:D005221), Pericardial Diseases (MESH:D008476), fibrosis (MESH:D005355), malignancy (MESH:D009369), peptic ulcer disease (MESH:D010437), LGE (MESH:C564835)
- **Chemicals:** steroids (MESH:D013256), colchicine (MESH:D003078), gadolinium (MESH:D005682), prednisone (MESH:D011241), F-18 fluorodeoxyglucose (MESH:D019788), prednisolone (MESH:D011239), BioRender (-)
- **Species:** Mycobacterium intracellulare subsp. intracellulare (subspecies) [taxon 35617], Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12823680/full.md

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Source: https://tomesphere.com/paper/PMC12823680